Previous work has shown that an origin-deficient YAC (5ORIdeltaYAC) induces a novel checkpoint. This checkpoint is independent of DNA damage. It is also different from the HU-induced replication checkpoint because replication forks do not stall and Rad53 is not activated. Therefore, it was postulated that this novel checkpoint monitors ongoing DNA synthesis. Interestingly, Rad9 was found essential for maintaining this checkpoint, indicating a previously unknown role of Rad9 in monitoring S phase progression in a normal cell cycle. A genetic screen will be conducted to identify additional components of this novel checkpoint pathway. This work will contribute to our understanding of how checkpoint mechanisms operate during an unperturbed cell cycle. It will also further our understanding of how cancer cells escape cell cycle and checkpoint control, leading to genome instability.